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    Interleukin-receptor antagonist and tumour necrosis factor inhibitors for the primary and secondary prevention of atherosclerotic cardiovascular diseases
    (Wiley, 2024-09-19)
    MARTI CARVAJAL, ARTURO JOSE  
    ;
    Mario A Gemmato-Valecillos
    ;
    Diana Monge Martín
    ;
    Mark Dayer
    ;
    Eduardo Alegría-Barrero
    Background: Atherosclerotic cardiovascular disease (ACVD) is worsened by chronic inflammatory diseases. Interleukin receptor antagonists (IL-RAs) and tumour necrosis factor-alpha (TNF) inhibitors have been studied to see if they can prevent cardiovascular events. Objectives: The purpose of this study was to assess the clinical benefits and harms of IL-RAs and TNF inhibitors in the primary and secondary prevention of ACVD. Search methods: The Cochrane Heart Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), Ovid MEDLINE (including In-Process & Other Non-Indexed Citations), Ovid Embase, EBSCO CINAHL plus, and clinical trial registries for ongoing and unpublished studies were searched in February 2024. The reference lists of relevant studies, reviews, meta-analyses and health technology reports were searched to identify additional studies. No limitations on language, date of publication or study type were set. Selection criteria: RCTs that recruited people with and without pre-existing ACVD, comparing IL-RAs or TNF inhibitors versus placebo or usual care, were selected. The primary outcomes considered were all-cause mortality, myocardial infarction, unstable angina, and adverse events. Data collection and analysis: Two or more review authors, working independently at each step, selected studies, extracted data, assessed the risk of bias and used GRADE to judge the certainty of evidence. Main results: We included 58 RCTs (22,053 participants; 21,308 analysed), comparing medication efficacy with placebo or usual care. Thirty-four trials focused on primary prevention and 24 on secondary prevention. The interventions included IL-1 RAs (anakinra, canakinumab), IL-6 RA (tocilizumab), TNF-inhibitors (etanercept, infliximab) compared with placebo or usual care. The certainty of evidence was low to very low due to biases and imprecision; all trials had a high risk of bias. Primary prevention:
IL-1 RAs 
The evidence is very uncertain about the effects of the intervention on all-cause mortality(RR 0.33, 95% CI 0.01 to 7.58, 1 trial), myocardial infarction (RR 0.71, 95% CI 0.04 to 12.48, I² = 39%, 2 trials), unstable angina (RR 0.24, 95% CI 0.03 to 2.11, I² = 0%, 2 trials), stroke (RR 2.42, 95% CI 0.12 to 50.15; 1 trial), adverse events (RR 0.85, 95% CI 0.59 to 1.22, I² = 54%, 3 trials), or infection (rate ratio 0.84, 95% 0.55 to 1.29, I² = 0%, 4 trials). Evidence is very uncertain about whether anakinra and cankinumab may reduce heart failure (RR 0.21, 95% CI 0.05 to 0.94, I² = 0%, 3 trials). Peripheral vascular disease (PVD) was not reported as an outcome. IL-6 RAs
The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 0.68, 95% CI 0.12 to 3.74, I² = 30%, 3 trials), myocardial infarction (RR 0.27, 95% CI 0.04 to1.68, I² = 0%, 3 trials), heart failure (RR 1.02, 95% CI 0.11 to 9.63, I² = 0%, 2 trials), PVD (RR 2.94, 95% CI 0.12 to 71.47, 1 trial), stroke (RR 0.34, 95% CI 0.01 to 8.14, 1 trial), or any infection (rate ratio 1.10, 95% CI: 0.88 to 1.37, I2 = 18%, 5 trials). Adverse events may increase (RR 1.13, 95% CI 1.04 to 1.23, I² = 33%, 5 trials). No trial assessed unstable angina. TNF inhibitors
The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 1.78, 95% CI 0.63 to 4.99, I² = 10%, 3 trials), myocardial infarction (RR 2.61, 95% CI 0.11 to 62.26, 1 trial), stroke (RR 0.46, 95% CI 0.08 to 2.80, I² = 0%; 3 trials), heart failure (RR 0.85, 95% CI 0.06 to 12.76, 1 trial). Adverse events may increase (RR 1.13, 95% CI 1.01 to 1.25, I² = 51%, 13 trials). No trial assessed unstable angina or PVD. Secondary prevention:
IL-1 RAs
The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 0.94, 95% CI 0.84 to 1.06, I² = 0%, 8 trials), unstable angina (RR 0.88, 95% CI 0.65 to 1.19, I² = 0%, 3 trials), PVD (RR 0.85, 95% CI 0.19 to 3.73, I² = 38%, 3 trials), stroke (RR 0.94, 95% CI 0.74 to 1.2, I² = 0%; 7 trials), heart failure (RR 0.91, 95% 0.5 to 1.65, I² = 0%; 7 trials), or adverse events (RR 0.92, 95% CI 0.78 to 1.09, I² = 3%, 4 trials). There may be little to no difference between the groups in myocardial infarction (RR 0.88, 95% CI 0.0.75 to 1.04, I² = 0%, 6 trials). IL6-RAs
The evidence is very uncertain about the effects of the intervention on all-cause mortality (RR 1.09, 95% CI 0.61 to 1.96, I² = 0%, 2 trials), myocardial infarction (RR 0.46, 95% CI 0.07 to 3.04, I² = 45%, 3 trials), unstable angina (RR 0.33, 95% CI 0.01 to 8.02, 1 trial), stroke (RR 1.03, 95% CI 0.07 to 16.25, 1 trial), adverse events (RR 0.89, 95% CI 0.76 to 1.05, I² = 0%, 2 trials), or any infection (rate ratio 0.66, 95% CI 0.32 to 1.36, I² = 0%, 4 trials). No trial assessed PVD or heart failure. TNF inhibitors
The evidence is very uncertain about the effect of the intervention on all-cause mortality (RR 1.16, 95% CI 0.69 to 1.95, I² = 47%, 5 trials), heart failure (RR 0.92, 95% 0.75 to 1.14, I² = 0%, 4 trials), or adverse events (RR 1.15, 95% CI 0.84 to 1.56, I² = 32%, 2 trials). No trial assessed myocardial infarction, unstable angina, PVD or stroke. Adverse events may be underestimated and benefits inflated due to inadequate reporting. Authors' conclusions: This Cochrane review assessed the benefits and harms of using interleukin-receptor antagonists and tumour necrosis factor inhibitors for primary and secondary prevention of atherosclerotic diseases compared with placebo or usual care. However, the evidence for the predetermined outcomes was deemed low or very low certainty, so there is still a need to determine whether these interventions provide clinical benefits or cause harm from this perspective. In summary, the different biases and imprecision in the included studies limit their external validity and represent a limitation to determining the effectiveness of the intervention for both primary and secondary prevention of ACVD.
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    Item type:Publication,
    Vasodilators for women undergoing fertility treatment
    (Wiley, 2018-10-12)
    Rosa B Gutarra-Vilchez
    ;
    Xavier Bonfill Cosp
    ;
    Demián Glujovsky
    ;
    VITERI GARCIA, ANDRES ALEJANDRO  
    ;
    Fernando M. Runzer-Colmenares
    Background: The rate of successful pregnancies brought to term has barely increased since the first assisted reproductive technology (ART) technique became available. Research suggests that vasodilators may increase endometrial receptivity, thicken the endometrium, and favour uterine relaxation, all of which could improve the chances of successful assisted pregnancy. Objectives: To evaluate the effectiveness and safety of vasodilators in women undergoing fertility treatment. Search methods: We searched the Cochrane Gynaecology and Fertility Group Specialised Register of controlled trials, CENTRAL, MEDLINE, Embase, three other databases, and two clinical trial registries in April 2024, with no language or date restrictions. We also searched grey literature sources and checked the reference lists of relevant articles. Selection criteria: We included randomised controlled trials (RCTs) comparing vasodilators (alone or combined with other treatments) versus placebo or no treatment or versus other agents in women undergoing fertility treatment. Data collection and analysis: Two review authors independently selected studies, assessed risk of bias, extracted data, and calculated risk ratios (RRs). We combined study data using a fixed-effect model and assessed evidence certainty using the GRADE approach. Our primary outcomes were live birth or ongoing pregnancy and vasodilator side effects. Our secondary outcomes were clinical pregnancy, endometrial thickness, multiple gestation, miscarriage, and ectopic pregnancy. Main results: We included 45 studies with a total of 4404 women. The included studies compared a vasodilator versus a placebo or no treatment (40 RCTs), vasodilators plus another agent versus placebo or no treatment (3 RCTs) or versus oestrogens (3 RCTs). The mean length of follow-up was 15.45 weeks. Overall, the certainty of evidence was very low to moderate. The main limitations were imprecision (low number of events and participants) and risk of bias (lack of blinding in studies that reported subjective outcomes). Vasodilators versus placebo or no treatment. Vasodilators may result in little to no difference in rates of live birth or ongoing pregnancy compared with placebo or no treatment (RR 1.21, 95% CI 0.93 to 1.58; I² = 0%; 6 RCTs, 740 women; low-certainty evidence), but probably increase overall rates of side effects (RR 2.14, 95% CI 1.55 to 2.98; I² = 0%; 7 RCTs, 668 women; moderate-certainty evidence). The evidence suggests that 246 per 1000 women achieve live birth or ongoing pregnancy with a placebo or no treatment, and 229 to 389 per 1000 will do so using vasodilators. Vasodilators compared with placebo or no treatment likely increase rates of clinical pregnancy (RR 1.45, 95% CI 1.28 to 1.64; I² = 22%; 25 RCTs, 2506 women; moderate-certainty evidence). Vasodilators compared with placebo or no treatment probably have little or no effect on rates of multiple gestation or birth (RR 1.37, 95% CI 0.73 to 2.55; I² = 0%; 7 RCTs, 763 women; moderate-certainty evidence), miscarriage (RR 1.01, 95% CI 0.59 to 1.74; I² = 0%; 8 RCTs; 829 women; moderate-certainty evidence), and ectopic pregnancy (RR 1.25, 95% CI 0.34 to 4.59; I² = 0%; 4 RCTs, 543 women; moderate-certainty evidence). Most studies found a beneficial effect of vasodilators for endometrial thickness, but the reported effect estimates varied (I² = 93%), from a mean difference of 0.47 mm higher (95% CI 0.90 mm lower to 1. 84 mm higher) to 1.94 mm higher (95% CI 1.37 higher to 2.51 mm higher), and the evidence was very uncertain. Hence, we are unsure how to interpret these results. Vasodilators versus oestrogens. Vasodilators compared with oestrogens may have little or no effect on rates of live birth or ongoing pregnancy (RR 0.83, 95% CI 0.30 to 1.33; 1 RCT, 44 women, low-certainty evidence). The evidence is very uncertain regarding the effect of sildenafil compared with oestrogens on clinical pregnancy rates (RR 0.99, 95% CI 0.71 to 1.38; I² = 59%; 3 RCTs, 262 women; very low-certainty evidence), endometrial thickness (RR 1.90, 95 CI 1.15 to 3.13; 1 RCT, 120 women; very low-certainty evidence) and miscarriage rates (RR 0.50, 95% CI 0.05 to 5.12; 1 RCT, 44 women; very low-certainty evidence). Authors' conclusions: Among women undergoing fertility treatment, there may be little or no difference in the rate of live birth or ongoing pregnancy in those who receive vasodilators compared with those who receive a placebo or no treatment, and compared with those who receive oestrogens. Compared with placebo or no treatment, vasodilators likely increase rates of clinical pregnancy, but probably also increase overall rates of side effects. The evidence on clinical pregnancy with vasodilators versus oestrogens is very uncertain, and we found no evidence on overall side effects for the comparison of vasodilators versus oestrogens. We are unsure about the effect of vasodilators versus placebo or no treatment and versus oestrogens on endometrial thickness. Vasodilators versus placebo or no treatment probably have little or no effect on multiple gestation or birth, miscarriage, and ectopic pregnancy. Future studies should be adequately randomised and powered to ensure a more accurate evaluation of each treatment, with live births as a primary outcome.